What Are the Signs of Glandular Fever?

Glandular fever is short for infectious mononucleosis. Glandular fever is an acute infectious disease caused by Epstein-Barr virus (EBV) infection. Clinically, it is characterized by fever, angina, lymph nodes, hepatosplenomegaly, increased lymphocytes in peripheral blood, and abnormal lymphocytes.

Glandular fever

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Glandular fever is short for infectious mononucleosis. Glandular fever is an acute infectious disease caused by Epstein-Barr virus (EBV) infection. Clinically, it is characterized by fever, angina, lymph nodes, hepatosplenomegaly, increased lymphocytes in peripheral blood, and abnormal lymphocytes.

Chinese name

Glandular fever

Foreign name

infectiousmononucleosis

Meaning

Infectious mononucleosis

Nature

Acute infectious disease

EBV belongs to the herpes virus group. It was first discovered in 1964 by Epstein and Barr from cell cultures of African malignant lymphomas. Virus globule

Shaped, about 180 nm in diameter, with a lipoprotein envelope attached to the surface of the capsid and a double-stranded DNA core.

The virus has very special growth requirements, so virus isolation is difficult. However, the virus can be detected in cultured lymphocytes by immunofluorescence or electron microscopy. EBV has B-cellophilic properties and can serve as its lysogen, turning B lymphocytes into lymphoblasts.

EBV has five antigenic components, namely the viral capsid antigen (VcA), membrane antigen (MA), early antigen (EA), complement-binding antigen (soluble antigen S), and nuclear antigen (EBNA). Various antigens can produce corresponding antibodies.

The disease occurs throughout the world and is mostly sporadic and can cause pandemics. The disease can occur throughout the year, mostly from late autumn to early spring. Patients and EBV carriers are the source of infection. The virus is abundant in salivary glands and saliva, and can continuously or intermittently detoxify for weeks, months, or even years. Transmission is mainly through oral contact (oral-to-oral transmission). Although droplet transmission is possible, it is not important. Even through blood transfusion and fecal transmission, there is still controversy about intrauterine transmission.

(1) Sources of infection The carriers and patients are the source of infection of the disease. The rate of infection in healthy people is about 15%.

(B) More than 80% of patients have EB virus in the nasopharynx, and 15 to 20% can recover from the throat for a long time after recovery. Oral and nasal close contact is the main route of transmission, and it can also be transmitted through droplets and blood transfusions.

(3) Vulnerable populations are generally susceptible, but children and adolescents are more common. Most children under 6 years of age suffer from recessive or mild onset. Infection over 15 years of age is typical. Permanent immunity can be obtained after the illness, and the second incidence is uncommon.

The pathogenesis has not been fully elucidated. EBV people may first proliferate in the lymphatic tissue of the pharynx after entering the mouth, and then enter the blood to cause viremia, which then affects the lymphatic system of the body. Because EBV receptors are on the surface of B cells, EBV mainly infects B cells, resulting in changes in B cell surface antigens, which in turn causes T-cell defense responses to form cytotoxic effector cells (CTLs) that directly destroy EBV infected B cells. A large number of abnormal lymphocytes in patients' blood (also known as atypical lymphocytes) are such killer CTLs. Therefore, it is more appropriate to call this disease "infectious atypical lymphocytosis" or "infectious mononucleosis". EBV can cause B-cell polyclonal activation and produce non-specific polyclonal immunoglobulins, some of which are characteristic of the disease, such as Paul-Bunnell heterophilic antibodies.

In addition to the interaction of B and T cells, the pathogenesis of this disease is also caused by immune pathological factors such as immune complex deposition and direct damage of the virus to cells. There are few typical cases in infants and young children, mainly due to inadequate immune response to EB virus.

As the infection progresses, the interaction of B and T lymphocytes leads to an increase in the activity of CTLs, macrophages and non-specific killer cells, hindering the proliferation of B cells, and ultimately controlling the disease, which reflects the self-limiting nature of the disease process. People with congenital and acquired immunodeficiency lack this immune mechanism, leading to uncontrolled B cell proliferation and even immunoblastic B cell sarcoma or other malignant lymphoproliferative diseases, such as Burkitt lymphoma.

The main pathological changes of this disease are benign hyperplasia of lymphatic tissue and lymphadenopathy, but no suppuration, high proliferation of lymphocytes and monocytes-phagocytic cells, and the proliferation of T cells in the thymus-dependent paracortical area is most significant. The liver, spleen, kidney, bone marrow, and central nervous system can all be affected, mainly by abnormal polymorphic lymphocyte infiltration.

Clinical manifestations 1. Fever without a certain fever type, body temperature of 37.5-40 ° C, lasting for 4 to 21 days, and usually fever reduction in about 1 week. It can also be low-temperature for up to 3 months.

(1) About 30% of patients in the respiratory system may be complicated by bacterial infection of the pharynx. Interstitial pneumonia can occur in about 5% of patients.

(B) Edema may occur in some patients with urinary complications. Nephritis-like changes such as proteinuria, urinary casts, and increased blood urea nitrogen, are mostly reversible. (C) Cardiovascular complications with myocarditis accounted for about 6%. ECG showed T wave inversion, low level and prolonged P-R interval.

(D) Meningitis, meningoencephalitis, and peripheral neuropathy can occur in neurological complications, and the incidence is about 1%.

Other complications include spleen rupture, hemolytic anemia, gastrointestinal bleeding, and parotid enlargement.

The diagnosis is based on typical clinical manifestations (fever, sore throat, hepatosplenomegaly and superficial lymph node enlargement), peripheral blood heteromorphic lymphocytes> 10%, and positive heterophilic agglutination tests, and clinical diagnosis can be made by combining epidemiological data. For patients with negative heterophilic agglutination test, specific EBV antibodies (VCAIgM, EAIgG) can be determined to help diagnosis.

This disease should be distinguished from the increase in monocytes caused by Mycoplasma pneumoniae, cytomegalovirus, adenovirus, hepatitis A virus infection, rubella, and herpetic pharyngitis. Among them, cytomegalovirus is the most common. Some people think that almost half of infectious mononucleosis negative for heterophile antibodies are related to CMV. Mediastinal lymphadenopathy should be distinguished from malignant diseases such as lymphoma.

I. General Therapy

Bed rest during the acute phase. Respiratory isolation. Pay attention to oral hygiene. Ensure nutrition and sufficient calories. Symptomatic treatment.

Second, metronidazole

15-50mg / kg / d, taken orally in 3 times, and taken for 5-7 days, suitable for pharyngeal isthmus inflammation.

Third, antibiotics

People with bacterial infections should be given antibiotics (avoid ampicillin to avoid skin rashes).

Fourth, adrenal corticosteroids

Prednisone or dexamethasone is suitable for patients with severe symptoms of throat edema, respiratory tract obstruction, myocarditis, acute hemolytic anemia, thrombocytopenic purpura or poisoning. The course of treatment is generally 1-2 weeks.

Five, biological agents

The serum of patients during the recovery period was 10-20m1, intramuscular injection. Gamma globulin is injected intramuscularly or intravenously. Q-interferon 1 million U / d, intramuscular injection for 5 days.

Six, Chinese medicine

Proprietary medicines include antiviral oral solution, Yinhuang oral solution, Qingrejiedu oral solution, Golden Lotus tablets, Chuanxinlian tablets, etc., which should be treated according to symptoms.

Seven, antiviral western medicine

Acyclovir (Acyclovir) 10-20mg / kg / d, divided into 2-3 times, intravenously. Inhibit EBV replication, patients can continue to discharge virus in the nasopharynx after drug withdrawal. Ribavirin 10-15mg / kg / d, two intramuscular injections, 3 to 6 days and 1 course of treatment; or Wilostar oral solution (10ml each containing Ribavirinl 50mg), dose 1ml / kg / d, divided 2-3 Orally.

Eight, severe complications treatment

Surgery should be performed if the spleen is ruptured, and tracheostomy should be performed when needed.

The prognosis of this disease is mostly good. The course of disease is usually 1 to 2 weeks, but there may be relapses. Some patients have low fever, enlarged lymph nodes, fatigue, and weakness after the disease for several weeks or months. In rare cases, the course of the disease has been extended for several years. The case fatality rate is 1% to 2%. The death is due to spleen rupture, meningitis, myocarditis, and so on. People with congenital immunodeficiency infected with the disease quickly deteriorated and died. This disease and malignant lesions of the monocyte macrophage system are two very different diseases. Although EB virus is also found in patients with lymphoma, the disease does not turn into lymphoma.

EB virus vaccines are being developed at home and abroad. In addition to being used to prevent this disease in the future, EBV infection-related childhood malignant lymphoma and nasopharyngeal carcinoma are also being considered for immunological prevention.